Following a unilateral lesion of the rat nucleus basalis of Meynert, there was an acute (1 week) increase in the number of neocortical M2 muscarinic binding sites which returned to normal after 3 months. Neocortical M1 muscarinic binding sites were normal at 1 week but decreased at 3 months. These changes were bilateral and suggest that bilateral changes in cortical cholinergic receptors follow unilateral degeneration of cholinergic input. The differentiation of adrenergic derivatives of the rat neural crest was examined using the glucocorticoid receptor (GR) as the molecular marker. Both adrenal and extra-adrenal chromaffin cells were found to have similar temporal patterns of GR localization and responsiveness to dexamethasone during postnatal development, while these same characteristics were not found in sympathetic neurons. In stretozotocin (STZ)-treated diabetic rats, adrenal tyrosine hydroxylase (TH). dopamine beta-hydroxylase (DBH) and phenylethanolamine N-methyltransferase (PNMT) activities were all increased as were concentrations of dopamine, norepinephrine and epinephrine. Binding of (3H)prazosin and (3H)dihyroalprenolol to myocardial adrenergic receptors were decreased. These results suggest that catecholaminergic abnormalities may contribute to metabolic deficits in diabetes mellitus. Nerve growth factor (NGF) receptors were identified in the human cerebral cortex and had a dissociation constant (Kd) of 150-300 pM. The binding of (125I)-NGF to membranes prepared from Alzheimer's disease brains did not differ significantly from binding in normal brains. Immunocytochemistry with polyclonal antibodies, demonstrated for plasma proteins in normal formalin-fixed brain tissue in a number of subcortical regions, including the nucleus basalis, thalamus, hypothalamus, dentate nucleus and spinal cord. Only a few pyramidal neurons in cortical layers III and V were positive.